I am interested in how F. diplosiphon regulates its phycocyanin genes as a response to light color and nutrient level.In replete conditions cells express PC1 and PC2 (red light only) phycocyanin, which form the specific discoid structures of the phycobilisome rods. When the level of sulfur in the medium decreases the cells start producing the PC3 phycocyanin at the expense of PC1 and PC2. At the amino acid level, PC3 lacks most of the sulfur-containing residues when compared to PC1 and PC2. This reversible process presumably allows cells to store the essential sulfur macronutrient in their antennae proteins, which are one the most abundant component of their proteome, while still performing the light-harvesting function. In its freshwater environment, F. diplosiphon may use this strategy to acclimate to the existing fluctuations of sulfate.

We found that regulation of phycocyanin genes by sulfur level takes place at both transcriptional and posttranscriptional level. We are using a number of genetic and molecular biology techniques to dissect the mechanisms through which this control is carried out.

In addition, I am also researching how F. diplosiphon controls its green light response at the level of cpeCDESTR operon apart from the contribution of Rca signaling system. In red light, the cpeC operon is down-regulated by both Rca and by Cgi system. Cgi was found to act posttranscriptionally. I found several mutants that are defective in down-regulation of the cpeC operon and experiments are underway to identify the mechanisms through which the mutated components operate.